Mechanisms of lung injury.
The adult respiratory distress syndrome is pulmonary edema with low heart pressures and hypoxemia. Based on experimental models of the human disease, it is likely that functional injury to the lung includes pulmonary vasoconstriction, a loss of hypoxic vasoconstriction, increases in resistance to airflow across the lungs, decreases in lung compliance (perhaps both resulting from airway constriction), and lung microvascular injury resulting in pulmonary edema. Data accumulated over the last several years strongly suggest an important role for both cyclo-oxygenase metabolites and lipoxygenase metabolites of arachidonic acid in mediating lung vascular injury in this syndrome. Likewise, more recent evidence suggests a causative role for granulocytes in mediating the lung injury. Based on what is known about the biological activity of products of granulocytes and metabolites of arachidonic acid, it is reasonable to hypothesize a sequence of events in which arachidonate metabolites and granulocytes interact to result in pulmonary vasoconstriction, loss of hypoxic vasoconstriction, airway responses and capillary injury. It remains possible, perhaps even likely, that other humoral mediators, platelets and perhaps even other cellular mediators (for example, mast cells or lymphocytes) participate in the pathogenic sequence of events in ARDS. Specific delineation of the mechanisms of lung injury in this syndrome must await further research.
D000328:Adult; D000403:Airway Resistance; D000818:Animals; D001095:Arachidonic Acids / Q000378:metabolism; D002199:Capillary Permeability; D006098:Granulocytes / Q000502:physiology; D006801:Humans; D008084:Lipoxygenase; D008168:Lung / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology*; D008833:Microcirculation / Q000503:physiopathology; D012128:Respiratory Distress Syndrome / Q000209:etiology*
D001095:Arachidonic Acids; D008084:Lipoxygenase